A mutant strain of mouse FM3A cells defective in apoptotic DNA fragmentation.
A mutant strain of mouse FM3A cells was defective in apoptotic DNA fragmentation. Upon DNA damage by UV-radiation, the strain did not form DNA fragments, though it accumulated a large amount of p53 protein as did wild-type cells. No DNA fragmentation was observed when the strain was subjected to other kinds of DNA damaging agents such as X ray-radiation, or addition of etoposide to the culture medium. Other well-known biological stimulations inducing apoptosis, serum depletion or addition of TNF-alpha to the culture medium, also failed to cause DNA fragmentation in the cells. Using this apoptosis-deficient strain, we characterized another apoptotic reaction, export of phosphatidylserine to the cell surface. This molecule was exported onto the surface in both wild-type and the mutant cells when cells were treated with TNF-alpha and cycloheximide. Thus, the export of phosphatidylserine is suggested to be independent of the pathway for apoptotic DNA fragmentation.
Yamauchi
Y
Y
Cellular Physiology Laboratory, Institute of Physical and Chemical Research (RIKEN), Saitama, Japan.
Tanaka
A
A
Hanaoka
F
F
Okumura
K
K
D000818:Animals; D017209:Apoptosis / Q000528:radiation effects*; D002460:Cell Line; D003513:Cycloheximide / Q000494:pharmacology; D004249:DNA Damage / Q000528:radiation effects; D053938:DNA Fragmentation / Q000528:radiation effects*; D005047:Etoposide / Q000494:pharmacology; D005434:Flow Cytometry; D007700:Kinetics; D051379:Mice; D010718:Phosphatidylserines / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism; D014466:Ultraviolet Rays / Q000009:adverse effects; D014965:X-Rays / Q000009:adverse effects
D010718:Phosphatidylserines; D014409:Tumor Necrosis Factor-alpha; D016159:Tumor Suppressor Protein p53; D005047:Etoposide; D003513:Cycloheximide